Trinity College Dublin has a new insight into the role interleukin-36 (IL-36) plays as an immune distress signal may lead to new therapeutic approaches for psoriasis, according to a paper published online ahead of print in Cell Reports (Feb. 2, 2016; 14:1-15)
In the study, the investigators describe a process they have observed that causes IL-36 to switch to an active form when injury or infection damages tissue, triggering an inflammatory response.
The research team, led by the university’s Smurfit Professor of Medical Genetics, Seamus Martin, PhD, have identified proteases which alter IL-36, causing it to signal the immune system for inflammation, according to the paper. As well, they have found that these proteases are overactive in individuals with psoriasis, possibly representing a new target for treatment.
The authors found that activated neutrophils can release cathepsin G, elastase, and proteinase-3, which differentially activate IL-36 alpha, beta, and gamma. The authors also note that cathepsin G activity is elevated in human psoriatic lesions.
In a press release, professor Martin said “This discovery is very exciting and we really hope to develop this approach into a new way of treating psoriasis.”
“This work represents an excellent example of how basic research leads to fundamental breakthroughs in our understanding of how diseases arise. Without such knowledge, it would be very difficult to develop new therapies.”
Professor Martin said he and his team are grateful for the support provided by Science Foundation Ireland, who funded the study.